Traumatic brain injury (TBI) is a leading cause of death and disability in the United States. After primary injury, cerebral ischemia/hypoxia are major devastating complications. Early detection of brain tissue at risk for cerebral ischemia and hypoxia is the key to preventing secondary injury. Nuclear medicine also suggests that abnormal brain metabolism, measured as cerebral metabolic rate of oxygen (CMRO2), is associated with TBI patients' chronic atrophy and poor outcome. However, cerebral hemodynamics is region-specific; patients with normal intracranial and cerebral perfusion pressures can still have regional hypoxia. To date, there are no non- invasive tools to assess regional brain tissue for irreversible ischemic/hypoxia damage in critical care. In order to painta complete picture of the brain's hemodynamics, one needs to measure both arterial perfusion and venous oxygenation to calculate local cerebral blood flow (CBF), a measure for ischemia; brain tissue oxygenation, a measure for hypoxia; and CMRO2,. Recently, our group has developed an array of perfusion-weighted imaging (PWI) techniques to determine the arterial input function and further quantify absolute CBF more accurately than before. We further developed a quantitative susceptibility mapping technique, known as susceptibility weighted imaging and mapping (SWIM), to estimate blood oxygenation in major veins as a marker of draining tissue oxygenation. Unlike clinical catheter-based oxygenation monitor, which is invasive and restricted to one region, SWIM uses the major veins of the brain like embedded catheters to detect draining tissue oxygenation. More importantly, it is non-invasive, intrinsic, and abundant throughout the brain. A risk of regional hypoxia will render its draining veins with enhanced susceptibility on the SWIM map, indicative of low oxygenation. Using the relationship between arterial CBF and venous oxygenation, we can determine CMRO2, a key measure of brain tissue viability. Using both SWIM and PWI, we propose assessing brain tissue viability and its prognostic value in a cohort of 30 moderate to severe TBI patients in comparison with 30 demographically matched controls. We will first use a blood gas analyzer to validate and calibrate the SWIM estimation of blood oxygenation in an arm vein in all controls. Then, we will determine regional CBF, venous oxygenation, and CMRO2 levels throughout the brain at the acute stage in TBI patients. We will further determine the predictive value of regional hemodynamics at the acute stage for TBI patients' neurological and neuropsychological outcome at 6 months after injury, mediated by brain atrophy. The deliverable of this project will be a set of non-invasive imaging techniques for assessing brain tissue viability after TBI. The elucidation of cerebral hemodynamics will allow physicians to identify the brain tissue at risk for regional ischemia/hypoxia for proper treatment. This project is novel for its first time use of SWIM in TBI and non-invasive assessment of brain hemodynamics.